It is most probable that both genetic and environmental factors contribute to colon cancer etiology. At present, we have the capabilities to look at the interaction between dietary intake and genes which have been linked to colon cancer. In this study, we will obtain tumor tissue from cases enrolled in a large population-based case-control study of colon cancer (CA 48998). DNA will be extracted from tumor tissue and areas of p53 and K-ras genes will be analyzed at known mutational "hot spots," to determine the type and location of genetic mutations within the population of colon cancers. We also will evaluate the extent to which microsatellite instability occurs in colon tumors from this population-based study. We will evaluate the associations between these genetic mutations and tumor stage at diagnosis and survival. These data will be linked to environmental data, which includes extensive information on dietary intake within the population, to determine the impact that diet has on causing these somatic mutations (location and type of mutation). Total calories, fat, protein, calcium, fiber, beta carotene, and folic acid will be assessed with these genetic mutations, as will meats (along with method of and degree of cooking), dairy products, legumes, soy products, and fruits and vegetables. Other factors such as physical activity and body size which are closely related to dietary intake will be assessed both for their associations with somatic mutations. It is hypothesized that dietary intake (as specified above), physical inactivity, and a larger body size will contribute to somatic mutations of the p53 and K-ras genes and microsatellite instability. We also will store DNA frpom tumor tissue so that as laboratory techniques for analyzing somatic gene mutations necome refined, the associations between dietary intake and other genes, such as APC and DCC, can be assessed in the future.